Abstract
.Lipid composition of atherosclerotic plaques is considered to be highly related to plaque vulnerability. Therefore, a specific diagnostic or imaging modality that can sensitively evaluate plaques’ necrotic core is desirable in atherosclerosis imaging. In this regard, intravascular photoacoustic (IVPA) imaging is an emerging plaque detection technique that provides lipid-specific chemical information from an arterial wall with great optical contrast and long acoustic penetration depth. While, in the near-infrared window, a 1210-nm optical source is usually chosen for IVPA applications since lipids exhibit a strong absorption peak at that wavelength, the sensitivity problem arises in the conventional single-ended systems as other arterial tissues also show some degree of absorption near that spectral region, thereby generating undesirably interfering photoacoustic (PA) signals. A theory of the high-frequency frequency-domain differential photoacoustic radar (DPAR) modality is introduced as a unique detection technique for accurate and molecularly specific evaluation of vulnerable plaques. By assuming two low-power continuous-wave optical sources at and in a differential manner, DPAR theory and the corresponding simulation/experiment studies suggest an imaging modality that is only sensitive and specific to the spectroscopically defined imaging target, cholesterol.
Highlights
Atherosclerosis is a chronic cardiovascular disease (CVD) that is characterized by inflammation and the gradual buildup of lipid-rich plaque in the inner lining of the arterial walls.[1,2,3,4]
While the full risk factors or the cellular mechanism of plaque development are not yet fully understood, early atherosclerosis is initiated as lipid-carrying low-density lipoproteins (LDLs) get retained beneath the endothelial cells of the vessels.[2,3,4]
The retained LDLs get oxidized, and endothelial cells trigger the immune response by attracting monocyte-derived macrophages to the sites.[2,3,4]
Summary
Atherosclerosis is a chronic cardiovascular disease (CVD) that is characterized by inflammation and the gradual buildup of lipid-rich plaque in the inner lining of the arterial walls (intima).[1,2,3,4] While the full risk factors or the cellular mechanism of plaque development are not yet fully understood, early atherosclerosis is initiated as lipid-carrying low-density lipoproteins (LDLs) get retained beneath the endothelial cells of the vessels.[2,3,4] The retained LDLs get oxidized, and endothelial cells trigger the immune response by attracting monocyte-derived macrophages to the sites.[2,3,4] When the ingested lipids are not properly removed from macrophages by high-density-lipoproteins (HDLs), the internal level of the oxidized LDLs in macrophages increases abnormally and they transform into foam cells.[2,3,4] These foam cells eventually rupture causing local damage to the endothelial cells. More inflammatory processes follow to repair the injured endothelium by local cellular remodeling.[3,4] Cellular remodeling, may end up with some degree of misrepair; the corresponding local regions only become more prone to plaque formation. As more of these events occur, the development of plaque self-accelerates, and its size increases over time.[2,3,4]
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